| pubmed-article:18522544 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:18522544 | lifeskim:mentions | umls-concept:C1332717 | lld:lifeskim |
| pubmed-article:18522544 | lifeskim:mentions | umls-concept:C1706438 | lld:lifeskim |
| pubmed-article:18522544 | lifeskim:mentions | umls-concept:C0039194 | lld:lifeskim |
| pubmed-article:18522544 | lifeskim:mentions | umls-concept:C0450127 | lld:lifeskim |
| pubmed-article:18522544 | lifeskim:mentions | umls-concept:C0085358 | lld:lifeskim |
| pubmed-article:18522544 | lifeskim:mentions | umls-concept:C0038952 | lld:lifeskim |
| pubmed-article:18522544 | lifeskim:mentions | umls-concept:C1413244 | lld:lifeskim |
| pubmed-article:18522544 | lifeskim:mentions | umls-concept:C2698600 | lld:lifeskim |
| pubmed-article:18522544 | lifeskim:mentions | umls-concept:C0522536 | lld:lifeskim |
| pubmed-article:18522544 | lifeskim:mentions | umls-concept:C1512948 | lld:lifeskim |
| pubmed-article:18522544 | lifeskim:mentions | umls-concept:C0443252 | lld:lifeskim |
| pubmed-article:18522544 | pubmed:issue | 6 | lld:pubmed |
| pubmed-article:18522544 | pubmed:dateCreated | 2008-6-4 | lld:pubmed |
| pubmed-article:18522544 | pubmed:abstractText | Despite success of early islet allograft engraftment and survival in humans, late islet allograft loss has emerged as an important clinical problem. CD8+ T cells that are independent of CD4+ T cell help can damage allograft tissues and are resistant to conventional immunosuppressive therapies. Previous work demonstrates that islet allografts do not primarily initiate rejection by the (CD4-independent) CD8-dependent pathway. This study was performed to determine if activation of alloreactive CD4-independent, CD8+ T cells, by exogenous stimuli, can precipitate late loss of islet allografts. Recipients were induced to accept intrahepatic islet allografts (islet 'acceptors') by short-term immunotherapy with donor-specific transfusion (DST) and anti-CD154 mAb. Following the establishment of stable long-term islet allograft function for 60-90 days, recipients were challenged with donor-matched hepatocellular allografts, which are known to activate (CD4-independent) CD8+ T cells. Allogeneic islets engrafted long-term were vulnerable to damage when challenged locally with donor-matched hepatocytes. Islet allograft loss was due to allospecific immune damage, which was CD8- but not CD4-dependent. Selection of specific immunotherapy to suppress both CD4- and CD8-dependent immune pathways at the time of transplant protects islet allografts from both early and late immune damage. | lld:pubmed |
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| pubmed-article:18522544 | pubmed:language | eng | lld:pubmed |
| pubmed-article:18522544 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:18522544 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:18522544 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:18522544 | pubmed:month | Jun | lld:pubmed |
| pubmed-article:18522544 | pubmed:issn | 1600-6143 | lld:pubmed |
| pubmed-article:18522544 | pubmed:author | pubmed-author:GanEE | lld:pubmed |
| pubmed-article:18522544 | pubmed:author | pubmed-author:BumgardnerG... | lld:pubmed |
| pubmed-article:18522544 | pubmed:author | pubmed-author:LunsfordK EKE | lld:pubmed |
| pubmed-article:18522544 | pubmed:author | pubmed-author:HorneP HPH | lld:pubmed |
| pubmed-article:18522544 | pubmed:author | pubmed-author:KoesterM AMA | lld:pubmed |
| pubmed-article:18522544 | pubmed:author | pubmed-author:EiringA MAM | lld:pubmed |
| pubmed-article:18522544 | pubmed:author | pubmed-author:JayanshankarK... | lld:pubmed |
| pubmed-article:18522544 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:18522544 | pubmed:volume | 8 | lld:pubmed |
| pubmed-article:18522544 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:18522544 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:18522544 | pubmed:pagination | 1113-28 | lld:pubmed |
| pubmed-article:18522544 | pubmed:dateRevised | 2011-7-28 | lld:pubmed |
| pubmed-article:18522544 | pubmed:meshHeading | pubmed-meshheading:18522544... | lld:pubmed |
| pubmed-article:18522544 | pubmed:meshHeading | pubmed-meshheading:18522544... | lld:pubmed |
| pubmed-article:18522544 | pubmed:meshHeading | pubmed-meshheading:18522544... | lld:pubmed |
| pubmed-article:18522544 | pubmed:meshHeading | pubmed-meshheading:18522544... | lld:pubmed |
